ArticleBritish journal of cancer2000
Abnormalities of the FHIT gene in human oral carcinogenesis.
Article in British journal of cancer, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 50 citations in OpenAlex.
- Single-cell and Mendelian analyses reveal shared mechanisms between head and neck neoplasms and aging.Discover oncology · 2026Article
- Loss of Heterozygosity in Oral Potentially Malignant Disorders and Oral Squamous Cell Carcinoma - A Scoping Review.Head and neck pathology · 2025Article
- Article
- Chromosomal imbalances in oral squamous cell carcinoma: examination of 31 cell lines and review of the literature.Oral oncology · 2008Review
- A novel approach to simultaneously scan genes at fragile sites.BMC cancer · 2006Article
- Molecular predictors of clinical outcome in patients with head and neck squamous cell carcinoma.International journal of experimental pathology · 2005Review
- Cancer and the FRA3B/FHIT fragile locus: it's a HIT.British journal of cancer · 2003Article
- Loss of FHIT protein expression correlates with disease progression and poor differentiation in gastric cancer.Journal of cancer research and clinical oncology · 2003Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The abnormalities of the fragile histidine triad (FHIT) gene in tissue samples of oral squamous cell carcinomas (SCCs) along with several leukoplakias and an erythroplakia were examined to determine whether the FHIT gene is actually a frequent target in vivo for alteration during oral carcinogenesis. Abnormal transcripts of the FHIT gene were found in eight of 15 oral SCCs. Although these abnormal transcripts varied widely, deletion patterns incorporating a deletion of exon 5 were the most common. Loss of heterozygosity (LOH) analysis demonstrated that the abnormal FHIT transcripts found in cancer cells were attributable to abnormalities of the FHIT gene. Abnormal FHIT transcripts were also observed in two of seven premalignant lesions. Interestingly, in the case of one patient with a premalignant lesion showing an abnormal FHIT transcript, subsequent oral SCC developed during a 3-year follow-up period. On the other hand, in the two patients from whom both leukoplakia and SCC samples were taken simultaneously, abnormal FHIT transcripts were found only in the SCCs. Although the functional role of FHIT remains to be clarified, these results suggest that the FHIT alteration is actually involved in carcinogenesis of the oral epithelium.
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